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Cardiovascular Disease

Cellular Medicine in Cardiovascular Disease

Dr. Rath's discovery of the vitamin C-heart disease connection provides a new understanding of how heart disease and atherosclerosis develop, as well as the scientific foundation for developing effective natural and safe solutions.

Dr. Rath's research revealed that atherosclerosis and cardiovascular disease develop from the same cause as clinical scurvy – an arterial wall deficiency of vitamin C. Humans, unlike most animals, cannot synthesize vitamin C and, thus, rely on dietary intake of this nutrient. Chronic vitamin C deficiency leads to instability of blood vessel walls, and is secondary to the development of millions of small lesions and cracks in the artery wall, especially in the highly stressed coronary arteries. Production of cholesterol and other repair factors increases to repair the damage, particularly in the coronary arteries. In chronic vitamin deficiency, the repair process overcompensates and atherosclerotic plaques develop in the damaged areas.

Certain drastic behavioral modifications by arterial wall smooth muscle cells (SMC) have been considered key steps in the formation of atherosclerotic lesions. These include the massive migration of SMC from the inner layer of the vessel wall, increased proliferation of SMC (similar to a cancer-type growth), and the increased secretion of inflammatory- mediating enzymes called cytokines. These events occur over time, leading to the progressive development of atherosclerotic plaques. The synergistic effect of a specific nutrient mixture containing ascorbic acid, lysine, proline and a green tea extract has been shown to inhibit the atherogenic response of vascular smooth muscle cells to pathological stimuli, thus blocking the development of atherosclerotic lesions.

Unified theory of Human Cardiovascular Disease Leading the Way to the Abolition of this Disease as a Cause for Human Mortality
M. Rath, l. Pauling. Journal of Orthomolecular Medicine.7:5-15
In contrast to current therapeutic approaches, which target individual pathomechanisms or specific risk factors for CVD, this paper proposes a unified pathogenetic and therapeutic approach based on genetic, metabolic, evolutionary and clinical evidence - ascorbate deficiency. Chronic ascorbate deficiency leads to loosening of the connective tissue in the vascular wall and compensatory deposition of Lp(a) (lipoprotein(a)) and fibrinogen/fibrin.

Solution to Puzzle of Human Evolution
M. Rath, Journal of Orthomolecular Medicine. 7:73-80
This article discusses the rationale for the proposal that the underlying genetic precondition for the evolution of man was the loss of endogenous ascorbate production about 40 million years ago. This genetic mutation became the basis of the dramatic acceleration of human evolution and a quadruplication of the brain size in the recent 2.5 million years. Scurvy, the greatest threat to evolutionary survival of ascorbate-deficient man during the Ice Age, led to survival genetic features: Lp(a) for stabilizing the vascular wall and apo(a) to increased brain size, intelligence and fertility.

A New Era in Medicine
M. Rath. Journal of Orthomolecular Medicine. 8:134-135
This article proposes that, in contrast to the past, the 21st century will see eradication of major diseases, such as CVD, and establishment of nutritional medicine as an essential part of the healthcare system. Skepticism and bias against nutritional supplements will be replaced by acceptance of vitamins and essential nutrients as safe and affordable preventative and therapeutic agents, based on objective scientific attitude towards nutrient medical research.

Atherosclerosis

Nutrient Synergy – A Mixture of Ascorbic Acid, Lysine, Proline, Arginine, Cysteine and Green Tea Extract, Suppresses Autocrine Inflammatory Response in Cultured Human Aortic Smooth Muscle Cell
V. Ivanov, S. Ivanova, M.W. Roomi, S.P.Netke, A. Niedzwiecki, M. Rath
Presented at: 12th International Congress on Cardiovascular Pharmacotherapy, Barcelona, Spain, May 7-10, 2003
In this study, the synergistic anti-atherogenic effects of nutrients such as ascorbic acid, lysine, proline, arginine, cysteine, and epigallocatechin gallate (from green tea extract) were investigated in cultured human aortic smooth muscle cell (SMC) by measuring SMC growth rate, invasiveness, matrix metalloproteinase-2 (MMP-2) expression, and secretion of monocyte chemoattractant protein-1 (MCP-1) and interleukin-6 (IL-6). By inhibiting the atherogenic response of vascular smooth muscle cells to pathological stimuli, Nutrient Synergy blocks the development of atherosclerotic lesions.

Anti-Atherogenic Effects of a Mixture of Ascorbic Acid, Lysine, Proline, Arginine, Cysteine and Green Tea Phenolics in Human Aortic Smooth Muscle Cell
Ivanov V., Ivanova S., Roomi M.W., Netke S..P, Niedzwiecki A., Rath M.
Presented at: 12th International Congress on Cardiovascular Pharmacotherapy, Barcelona, Spain, May 7-10, 2003
In this study, the synergistic anti-atherogenic effects of nutrients such as ascorbic acid, lysine, proline, arginine, cysteine, and epigallocatechin gallate (from green tea extract) were investigated in cultured human aortic smooth muscle cell (SMC) by measuring SMC growth rate, invasiveness, matrix metalloproteinase-2 (MMP-2) expression, and secretion of monocyte chemoattractant protein-1 (MCP-1) and interleukin-6 (IL-6). By inhibiting the atherogenic response of vascular smooth muscle cells to pathological stimuli, Nutrient Synergy blocks the development of atherosclerotic lesions.

Plasmin-Induced Proteolysis and the Role of Apoprotein(a), Lysine, and Synthetic Lysine Analogs
M. Rath, L. Pauling. Journal of Orthomolecular Medicine. 7:17-23
Proteolytic degradation of extracellular matrix (ECM) by the protease plasmin is a universal mechanism, determining human health and disease. Under physiological conditions, this leads to cell migration and organ remodeling; under pathological conditions, to sustained degradation of the ECM, as associated with cancer and viral spread, as well as cardiovascular disease. In this paper, apoprotein(a), lysine and synthetic lysine analogs are discussed as inhibitors of plasmin-induced proteolysis and proposed as natural therapeutic options.

Reducing the Risk for Cardiovascular Disease with Nutritional Supplements
M. Rath. Journal of Orthomolecular Medicine. 7:153-16.2
This paper discusses the pathomechanisms for development of CVD and proposes the therapeutic use of ascorbate, niacin, L-proline, L-lysine and natural antioxidants for cardiovascular disease, based on their anti-atherosclerotic therapeutic actions such as releasing lipoprotein-a from the vascular wall

Solution to the Puzzle of Human Cardiovascular Disease: Its Primary Cause is Ascorbate Deficiency, Leading to the Deposition of Lipoprotein(a) and Fibrinogen/Fibrin in the Vascular Wall
M. Rath, L. Pauling. Journal of Orthomolecular Medicine. 6:125-134.
This article proposes that human cardiovascular disease is primarily a degenerative disease, resulting from the accumulation of lipoprotein(a), which is increased by low ascorbate concentrations. Ascorbate deficiency results from the inability of humans to synthesize endogenous ascorbate combined with an insufficient dietary ascorbate intake. Chronic ascorbate deficiency leads to extracellular accumulation of lipoprotein(a) and fibrinogen/fibrin, the hallmarks of the atherosclerotic lesion.

Aoprotein(a) is an Adhesive Protein
M. Rath. Journal of Orthomolecular Medicine. 6:139-143.
Apoprotein(a) plays important physiological roles as an adhesive protein in organizing the interaction between cellular systems and the extracellular matrix in tissue formation, remodeling, and repair. The importance of these roles is enhanced under pathological conditions, such as ascorbate deficiency, as it mediates the cellular-extracellular interaction during chronic repair processes.

Lipoprotein (a) is a Surrogate for Ascorbate
M. Rath. Proceedings of the National Academy of Sciences. 87: 6204-6207.
The concept that lipoprotein(a) is a surrogate for ascorbate is suggested by the fact that this lipoprotein is found generally in the blood of primates and the guinea pig, which have lost the ability to synthesize ascorbate, but only rarely in other animals. Properties shared with ascorbate, in accordance with this hypothesis, are acceleration of wound healing and of cell-repair mechanisms, strengthening of extracellular matrix (as in blood vessels), and prevention of lipid peroxidation. Evidence supporting this hypothesis is discussed.

Immunological Evidence for the Accumulation of Lipoprotein(a) in the Atherosclerotic Lesion of the Hypoascorbemic Guinea Pig
M. Rath. Proceedings of the National Academy of Sciences. 87: 9388-9390.
Atherosclerosis was induced in three guinea pigs by dietary ascorbate depletion. Using SDS/PAGE and subsequent immunoblotting, Lp(a) was identified as accumulating in the atherosclerotic plaque. Furthermore, adequate amounts of ascorbate (40 mg/kg body weight/day) prevented development of atherosclerotic plaques and accumulation of Lp(a). Guinea pigs were chosen for this study as, similar to humans, they lack endogenous ascorbate production

Antiatherosclerotic Effect of Probucol in WHHL Rabbits: Are There Plasma Parameters to Evaluate this Effect?
B. Finckh, A. Niendorf, M. Rath, U. Biesiegel. Arteriosderosis 9: 579-592.
To study the anti-oxidative activity of probucol (a lipid-lowering agent) and its influence on plaque development, the animal model of the LDL-receptor-defective Watanabe heritable hyperlipidemic (WHHL) rabbit was used. In addition to assessment of biochemical levels (lipid, probucol, alpha and beta tocopherol, and thiobarbituric reactive substances), the plaque areas were macroscopically and microscopically evaluated. Probucol decreased the progression of atherosclerotic plaques by way of a combined lipid-lowering and antioxidative effect.

HRT and Heart Disease

Enhancement of Cardio-Protective Effects and Attenuation of Adverse Effects of Female Sex Hormones on Cultured Human Vascular Smooth Muscle Cells by a Combination of Ascorbic Acid, Lysine, Proline, Arginine, Cysteine and Epigallocatechin
V. Ivanov, S. Ivanova, M. W. Roomi, S. P. Netke, A. Niedzwiecki, M. Rath.
Presented at: European Congress of Endocrinology, Lyon, France, April 26-30, 2003
Large numbers of menopausal women are using hormone replacement therapy (HRT) for counteracting such adverse effects as hot flashes and loss of bone mass. However, HRT has been recently shown to have major adverse effects on cardiovascular health. When tested in an experimental system of cultured human vascular smooth muscle cells, female sex hormones: produced diverse effects on such atherogenic changes in smooth muscle cells properties as pathologically increased growth rate and invasiveness, and excessive production of extracellular matrix components and inflammatory SW Nutrient Synergy enhanced cardio-protective action of female sex hormones and counteracted their adverse effects at these experimental conditions, suggesting it has great potential as an adjunctive therapeutic agent in inhibiting adverse effects and enhancing the cardio-protective effects of female sex hormones in HRT.